Inhibition of BET Bromodomain Targets Genetically Diverse Glioblastoma
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Reid C Thompson | Stefan Knapp | Susanne Muller | S. Knapp | R. Thompson | K. Lu | S. Muller | Jialiang Wang | Zhixiang Cheng | Yuanying Gong | Yufang Ma | Kaihua Lu | Xiang Lu | Larry A Pierce | L. Pierce | Yuanying Gong | Zhixiang Cheng | Jialiang Wang | Yufang Ma | Xiang Lu
[1] Julio E. Agno,et al. Small-Molecule Inhibition of BRDT for Male Contraception , 2012, Cell.
[2] Debyani Chakravarty,et al. Intratumoral heterogeneity of receptor tyrosine kinases EGFR and PDGFRA amplification in glioblastoma defines subpopulations with distinct growth factor response , 2012, Proceedings of the National Academy of Sciences.
[3] Sean J Morrison,et al. Cancer stem cells: impact, heterogeneity, and uncertainty. , 2012, Cancer cell.
[4] Mark W. Dewhirst,et al. Glioma stem cells promote radioresistance by preferential activation of the DNA damage response , 2006, Nature.
[5] P. Bamborough,et al. Discovery and characterization of small molecule inhibitors of the BET family bromodomains. , 2011, Journal of medicinal chemistry.
[6] S. Hung,et al. Knockdown of p21Cip1/Waf1 enhances proliferation, the expression of stemness markers, and osteogenic potential in human mesenchymal stem cells , 2011, Aging cell.
[7] H. Varmus,et al. Sensitivity of human lung adenocarcinoma cell lines to targeted inhibition of BET epigenetic signaling proteins , 2012, Proceedings of the National Academy of Sciences.
[8] Santosh Kesari,et al. Malignant gliomas in adults. , 2008, The New England journal of medicine.
[9] Hui Wang,et al. c-Myc Is Required for Maintenance of Glioma Cancer Stem Cells , 2008, PloS one.
[10] S. Sathornsumetee,et al. Designer Therapies for Glioblastoma Multiforme , 2008, Annals of the New York Academy of Sciences.
[11] Joshua M. Korn,et al. Comprehensive genomic characterization defines human glioblastoma genes and core pathways , 2008, Nature.
[12] Wei Zhang,et al. Gliomagenesis arising from Pten- and Ink4a/Arf-deficient neural progenitor cells is mediated by the p53-Fbxw7/Cdc4 pathway, which controls c-Myc. , 2013, Cancer research.
[13] R. Beddington,et al. Growth and Early Postimplantation Defects in Mice Deficient for the Bromodomain-Containing Protein Brd4 , 2002, Molecular and Cellular Biology.
[14] R. Henkelman,et al. Identification of human brain tumour initiating cells , 2004, Nature.
[15] C. Harley,et al. Neural Tumor-Initiating Cells Have Distinct Telomere Maintenance and Can be Safely Targeted for Telomerase Inhibition , 2010, Clinical Cancer Research.
[16] Gerald C. Chu,et al. Pten and p53 converge on c-Myc to control differentiation, self-renewal, and transformation of normal and neoplastic stem cells in glioblastoma. , 2008, Cold Spring Harbor symposia on quantitative biology.
[17] M. Dawson,et al. Cancer Epigenetics: From Mechanism to Therapy , 2012, Cell.
[18] A. Khayat,et al. c-MYC amplification and expression in astrocytic tumors , 2008, Acta Neuropathologica.
[19] Chi V Dang,et al. MYC on the Path to Cancer , 2012, Cell.
[20] B. Sullenger,et al. Notch Promotes Radioresistance of Glioma Stem Cells , 2009, Stem cells.
[21] R. Weinberg,et al. Growth-Inhibitory and Tumor- Suppressive Functions of p53 Depend on Its Repression of CD44 Expression , 2008, Cell.
[22] J. Aster,et al. BRD–NUT oncoproteins: a family of closely related nuclear proteins that block epithelial differentiation and maintain the growth of carcinoma cells , 2008, Oncogene.
[23] J. Sarkaria,et al. p16-Cdk4-Rb axis controls sensitivity to a cyclin-dependent kinase inhibitor PD0332991 in glioblastoma xenograft cells. , 2012, Neuro-oncology.
[24] A. Fisher,et al. Epigenetic signatures of stem-cell identity , 2007, Nature Reviews Genetics.
[25] Tzong-Shiue Yu,et al. A restricted cell population propagates glioblastoma growth after chemotherapy , 2012 .
[26] J. Brady,et al. The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription. , 2005, Molecular cell.
[27] P. Sandy,et al. Targeting MYC dependence in cancer by inhibiting BET bromodomains , 2011, Proceedings of the National Academy of Sciences.
[28] J. Sarkaria,et al. Establishment, Maintenance, and In Vitro and In Vivo Applications of Primary Human Glioblastoma Multiforme (GBM) Xenograft Models for Translational Biology Studies and Drug Discovery , 2011, Current protocols in pharmacology.
[29] Qiang Zhou,et al. Recruitment of P-TEFb for stimulation of transcriptional elongation by the bromodomain protein Brd4. , 2005, Molecular cell.
[30] C. Rice,et al. Suppression of inflammation by a synthetic histone mimic , 2010, Nature.
[31] S. Lowe,et al. RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia , 2011, Nature.
[32] Stephen L. Abrams,et al. Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways , 2011, Journal of cellular physiology.
[33] Stefan Knapp,et al. Bromodomains as therapeutic targets , 2011, Expert Reviews in Molecular Medicine.
[34] A. Belkina,et al. BET domain co-regulators in obesity, inflammation and cancer , 2012, Nature Reviews Cancer.
[35] S. Gabriel,et al. Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. , 2010, Cancer cell.
[36] P. Dennis,et al. Constitutive and inducible Akt activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells. , 2002, Molecular cancer therapeutics.
[37] Rebecca A Betensky,et al. Mosaic amplification of multiple receptor tyrosine kinase genes in glioblastoma. , 2011, Cancer cell.
[38] William B. Smith,et al. Selective inhibition of BET bromodomains , 2010, Nature.
[39] M. Prados,et al. Pharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts. , 2010, Cancer research.
[40] M. Esteller,et al. Cancer epigenetics reaches mainstream oncology , 2011, Nature Medicine.
[41] C. James,et al. Identification of molecular characteristics correlated with glioblastoma sensitivity to EGFR kinase inhibition through use of an intracranial xenograft test panel , 2007, Molecular Cancer Therapeutics.
[42] W. Cavenee,et al. Heterogeneity maintenance in glioblastoma: a social network. , 2011, Cancer research.
[43] Christopher J. Ott,et al. BET bromodomain inhibition targets both c-Myc and IL7R in high-risk acute lymphoblastic leukemia. , 2012, Blood.
[44] Yuri Kotliarov,et al. Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines. , 2006, Cancer cell.
[45] S. Robson,et al. Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia , 2011, Nature.
[46] Tony Kouzarides,et al. Targeting epigenetic readers in cancer. , 2012, The New England journal of medicine.
[47] R. Young,et al. BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc , 2011, Cell.
[48] Xiangyuan Wang,et al. Double bromodomain‐containing gene Brd2 is essential for embryonic development in mouse , 2009, Developmental dynamics : an official publication of the American Association of Anatomists.
[49] B. N. Devaiah,et al. BRD4 is an atypical kinase that phosphorylates Serine2 of the RNA Polymerase II carboxy-terminal domain , 2012, Proceedings of the National Academy of Sciences.